ZIC3 antibody - N-terminal region (ARP33504_P050)
- Known as:
- ZIC3 (anti-) - N-terminal region (ARP33504_P050)
- Catalog number:
- arp33504_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZIC3 antibody - N-terminal region (ARP33504_P050)
Related genes to: ZIC3 antibody - N-terminal region (ARP33504_P050)
- Gene:
- ZIC3 NIH gene
- Name:
- Zic family member 3
- Previous symbol:
- HTX1
- Synonyms:
- HTX, ZNF203
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-16
- Date modifiied:
- 2016-10-05
Related products to: ZIC3 antibody - N-terminal region (ARP33504_P050)
Related articles to: ZIC3 antibody - N-terminal region (ARP33504_P050)
- Defects in ZIC2, a member of the Zinc Finger of the Cerebellum family of transcription factors (TFs), cause holoprosencephaly, a congenital brain malformation characterized by the defective cleavage of cerebral hemispheres. However, the gene regulatory network (GRN) controlled by ZIC2 during neural development remains largely unexplored. Here, we combined a mouse embryonic stem cell (mESC) in vitro differentiation model toward anterior neural progenitors with genome editing and genomic methods to elucidate the ZIC2 GRN. We found that ZIC2 is dispensable in mESC due to compensation by ZIC3. In contrast, during neural induction ZIC2 directly controls the expression of master regulators implicated in the patterning and morphogenesis of specific brain regions (e.g. midbrain and roof plate). Mechanistically, ZIC2 plays a dual role in neural differentiation: during pluripotency exit, ZIC2 binds de novo to distal enhancers and increases their chromatin accessibility; during neural induction, ZIC2 is essential for the activation of a subset of the previously primed enhancers, which in turn control the expression of neural patterning regulators and signalling pathways (i.e. WNT) that prevent premature neuronal differentiation. Therefore, by sequentially acting as a promiscuous priming TF and selective enhancer activator, ZIC2 canalizes pluripotent cells toward neural progenitors with rostro-dorsal identities. - Source: PubMed
Mariner-Faulí MaríaSánchez-Gaya VíctorRobert Sarah MalikaRespuela Patriciade la Cruz-Molina SaraLobato-Moreno SaraTrovato MatteoPrummel Karin DNoh Kyung-MinZaugg Judith BRada-Iglesias Álvaro - Congenital heart disease (CHD) is the most common birth defect, and its pathogenesis is closely related to the abnormal establishment of the left-right (LR) bod axis, which highly depends on the ciliary function of the left-right organizer (LRO). This review systematically expounds the molecular pathways by which ciliary structural and functional abnormalities cause cardiac malformations by integrating multi-species model evidence. We believe that defects in multiple conserved genes (including , , , , , and microRNAs) disrupt ciliary assembly, motility, or signaling capacity, leading to the disappearance of the leftward nodal flow or mechanical sensing failure within the LRO. This further interrupts the left-specific calcium ion flicker and the activation of the Nodal-Pitx2 signaling cascade, ultimately resulting in failed cardiac looping and structural defects (such as ventricular septal defect and transposition of the great arteries). This review integrates transcriptional regulation, protein stability, miRNA-mediated fine regulation, and the planar cell polarity (PCP) pathway into a unified "cilia-LRO-heart" network and explores the molecular mechanisms of cilia in valve diseases and cardiac fibrosis. This not only deepens the understanding of the fundamental biological processes of heart development but also provides new molecular targets and theoretical frameworks for the genetic diagnosis and counseling of related congenital heart diseases. - Source: PubMed
Publication date: 2026/02/17
Ma WenqiZhang ZhuofengMa YunMa Chengxu - Brain microvascular endothelial cells (BMECs) forming the blood-brain barrier (BBB) maintain brain homeostasis through specialized properties such as tight junctions, efflux transporters, and low levels of transcytosis. However, mechanisms governing induction of BBB properties during development remain poorly understood. We mined single-cell RNA sequencing datasets to identify transcription factors (TFs) critical for BBB development. Forty-four TFs were overexpressed in human pluripotent stem cell-derived endothelial cells cultured in the presence of the Wnt pathway agonist CHIR99021 to identify TFs capable of directing acquisition of BBB properties via forward programming. Individual TFs, including , , , , , , , , , and , induced distinct BBB-like gene expression patterns. Combinations of these TFs induced many canonical BBB genes, yielding ECs with reduced endocytosis, increased efflux activity, and improved barrier function. The resultant forward programmed CNS-like ECs (fpCECs) offer promising tools for modeling human BBB development and neurovascular disease and for drug screening. - Source: PubMed
Publication date: 2026/02/02
Tamhankar SoniyaDing YunfengHashjin Fatemeh YaghoobiBoutom Sarah MDaneman RichardPalecek Sean PShusta Eric V - Evolutionary adaptation to diurnal vision in ground squirrels has led to the development of a cone-dominant retina, in stark contrast to the rod-dominant retinas of most mammals. The molecular mechanisms driving this shift remain largely unexplored. Here, we perform single-cell RNA sequencing and chromatin accessibility profiling (scATAC-Seq) across developmental retinal neurogenesis in the 13-lined ground squirrel (13LGS) to uncover the regulatory basis of this adaptation. We find that 13LGS cone photoreceptors arise not only from early-stage neurogenic progenitors, as seen in rod-dominant species like mice, but also from late-stage neurogenic progenitors. This extended period of cone generation is driven by a heterochronic shift in transcription factor expression, with cone-promoting factors such as , , and remaining active in late-stage progenitors, and factors that promote cone differentiation such as , , and expressed precociously in late-stage neurogenic progenitors. Functional analyses reveal that and are sufficient to promote cone and repress rod photoreceptor-specific gene expression and act through species-specific regulatory elements that drive their expression in late-stage progenitors. These results demonstrate that modifications to gene regulatory networks underlie the development of cone-dominant retinas and provide insight into mechanisms of sensory adaptation and potential strategies for cone photoreceptor regeneration in vision disorders. - Source: PubMed
Publication date: 2026/02/06
Weir KurtLyu PinKandoi SangeethaAn RoujinPannullo NicolePalazzo IsabellaTangeman Jared AShi JunDeVries Steven HMerriman Dana KQian JiangBlackshaw Seth - This study identified fibroblast-specific genes to develop a RiskScore model to improve prognostic accuracy and guide personalized treatment in glioblastoma (GBM). - Source: PubMed
Publication date: 2025/11/27
Liu NanZhao MingyueCui YetingZhao JiaxuanTu YanyangZhang TongcunHu Xiaofei